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目的:探讨正常、心衰时左心室内、外膜心肌细胞收缩舒张功能的差异。方法:采用主动脉缩窄术构建压力负荷型心衰小鼠。Langendorff灌流术分离小鼠左心室内、外膜心肌细胞。高速CCD摄像机系统和双激发荧光倍增系统同步测量内外膜心肌细胞肌小节收缩和胞内钙瞬变。张力传感器和微操作系统测量细胞的被动舒张张力(僵硬度)。结果:(1)正常小鼠内外膜收缩舒张功能存在差异,钙瞬变、钙Tau值、肌小节收缩幅度、僵硬度均为内膜大于外膜;(2)心衰时,小鼠左心室内外膜收缩舒张功能都受损,钙瞬变内外膜均降低,肌小节收缩幅度均减小,僵硬度均增大;(3)心衰时内外膜的钙瞬变差异消失,而肌小节收缩和僵硬度的差异依然存在。结论:正常心脏内膜是产生心肌收缩力的主要力量,心衰时内外膜细胞收缩舒张功能均受损,且内外膜本来存在的部分梯度差异在心衰时消失。
Objective: To investigate the difference of systolic and diastolic function in left ventricular and epicardial myocardium during normal and heart failure. Methods: Pressure-load heart failure mice were established by aortic constriction. Langendorff perfusion separation of mouse left ventricular and adventitial cardiomyocytes. High-speed CCD camera system and double-excited fluorescence doubler system simultaneous measurement of inner and outer membrane myocyte contractions and intracellular calcium transients. Tension sensors and micro-operating systems measure the passive diastolic tension (stiffness) of cells. Results: (1) There were differences in the diastolic and diastolic function of the inner and outer membrane in normal mice. The calcium transients, calcium Tau values, contractions of muscle segments and stiffness were both intima and adventitia. (2) Both inner and outer membrane contraction and diastolic function were impaired, calcium transient inner and outer membrane were reduced, the contractions of muscle segments were reduced, stiffness increased; (3) heart failure, the epicardium of the calcium transient disappearance of disappearance, and muscle contraction Differences in stiffness still exist. CONCLUSION: The normal cardiac endocardium is the main force that produces myocardial contractility. The systolic and diastolic functions of the cells in endocardium and epicardium are impaired in heart failure, and some differences in the original existence of the endocardium and adventitia are disappeared in heart failure.